CONCLUSION Oxidative and emotional stress may play a role in pathogenesis of PHG. Our study showed that serum oxidative stress and emotional stress were high in PHG. In other words, there was high systemic oxidative stress in PHG. © 2020 Wiley Periodicals, Inc.BACKGROUND Hair plays a significant role in shaping the appearance of an individual. Loss of hair can lead to serious effects on social esteem of an individual. The most common cause of hair loss is Androgenetic Alopecia (AGA).This hereditary disorder followed a specific pattern causing progressive thinning of hair in both Men and Women. AIMS The aim of the current study is to compare and evaluate the efficacy of QR678 therapy versus PRP in the treatment of Male Androgenetic Alopecia. Since QR678 and QR678 Neo have been found to be formulations equivalent in efficacy, the results would be the same with either formulation. METHODS A prospective, comparative, single&nbsp;blind study was carried out with 2 groups of 25 patients each. Intradermal injections of QR678 formulations and PRP were injected in group A and B respectively. Hair pull test, Video microscopic assessment, Global Photographic assessment was done and patient's subjective assessment was done through questionnaire at the end of the study. Results were evaluated after 6 months and follow up was done till 1 year. RESULTS 100% reduction in hair fall was noted at the end of 6 months in the QR678 group which was maintained for 1 year. Video microscopic evaluation showed that the hair density, terminal hair density, vellus hair density and shaft diameter were significantly better in QR678 group (P less then .005) than the PRP group. Since QR678 and QR678 Neo formulatons are equivalent in efficacy, the results of tthis trial can be attributed to be the same, irrespective of the formulation used. CONCLUSION The bioengineered formulation of QR678 proved to be more beneficial for Male Androgenetic Alopecia (Male pattern hair loss) compared to PRP. A comparative study between QR678 and PRP with long term follow&nbsp;up will widen our spectra of knowledge. © 2020 Wiley Periodicals, Inc.OBJECTIVE We explore here that memory loss observed in the early stage of Alzheimer's disease (AD) is a disorder of memory retrieval, instead of a storage impairment. This engram-centric explanation aims to enlarge the conceptual frame of memory as an emergent behavior of the brain and to propose a new treatment strategy for memory retrieval in dementia-AD. BACKGROUND The conventional memory hypothesis suggests that memory is stored as multiple traces in hippocampal neurons but recent evidence indicates that there are specialized memory engrams responsible for the storage and the retrieval of different memory types. UPDATED MEMORY HYPOTHESIS There are specialized memory engram neurons for each memory type and when information will be stored as a memory arrives in the hippocampus through afferent neurons finds its neuron according to the excitability states of engram neurons. The excitability level in engram neurons seems like a code canalizing the interactions between engrams and information. Therefore, to eneign object and its direct implantation into the brain may cause neuroinflammation, the main trigger of neurodegenerative diseases. Therefore, to test the engram hypothesis in human, new tools to allow specific engram activation should be discovered. © 2020 the Alzheimer's Association.Toll-like receptors (TLRs) build the first barrier in the innate immune response and therefore represent promising targets for the modulation of inflammatory processes. Recently, the pyrogallol-containing TLR2 antagonists CU-CPT22 and MMG-11 have been reported, however, their 1,2,3-tri-phenol motif renders them highly susceptible to oxidation and excludes them from use in extended experiments under aerobic conditions. Therefore, we have developed a set of novel TLR2 antagonists (1-9) based on the systematic variation of substructures, linker elements and the hydrogen-bonding pattern of the pyrogallol precursors by using chemically robust building blocks. https://www.selleckchem.com/products/2-nbdg.html The novel series of chemically stable and synthetically accessible TLR2 antagonists (1-9) was pharmacologically characterized and the potential binding modes of the active compounds were evaluated structurally. Our results provide novel insights into structure-activity relationships and allow&nbsp;for rationalization of structural binding characteristics. Moreover, it supports the hypothesis this class of TLR ligands bind solely to TLR2 and do not directly interact with TLR1 or TLR6 of the functional heterodimer. The most active compound from this series (6) , is chemically stable, non-toxic, TLR2-selective and shows a similar activity with regard to the pyrogallol starting points indicating the variability of the hydrogen bonding pattern. © 2020 WILEY-VCH Verlag GmbH &amp; Co. KGaA, Weinheim.In this work, we aimed to evaluate the adverse effects and the mechanism of intestinal barrier caused by titanium dioxide nanoparticles (TiO2 NPs). Here, the effects of two different dosages (300 and 1200?mg/kg) of TiO2 NPs on female mice (n = 5) were investigated. After 28-day oral exposure, the results of Ti content were significantly increased in the ileum in comparison with the control. The histopathological structure index of the ileum was significantly changed after TiO2 NPs exposure; villi height and crypt depth were decreased and increased, respectively. Meanwhile, TiO2 NPs treatment also significantly altered the transcription levels of genes. First, the GATA-3 and STAT-4 were upregulation and downregulation, respectively. Second, gene expressions of the Zonula Occludens-1, claudin (CLDN)-12, occludin, and myosin light chain kinase were significantly upregulated, while the CLDN-3 was decreased. Finally, the caspase-3, caspase-9, and caspase-12 were upregulated. The results of TUNEL staining indicated apoptosis in the ileum. In general, TiO2 NPs treatment significantly changed the intestine physical barrier in a dose-dependent manner. The toxicity of TiO2 NPs could be through the imbalance in the Th1/Th2. © 2020 Wiley Periodicals, Inc.